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Review
. 2015 Apr 1;7(4):a021287.
doi: 10.1101/cshperspect.a021287.

Adult neurogenesis in neurodegenerative diseases

Beate Winner  1 , Jürgen Winkler  2
Affiliations
Review

Adult neurogenesis in neurodegenerative diseases

Beate Winner et al. Cold Spring Harb Perspect Biol. .

Abstract

Adult neurogenesis is limited to specific brain regions in the mammalian brain, such as the hippocampal dentate gyrus and the subventricular zone/olfactory bulb system. Alterations in adult neurogenesis appear to be a common hallmark in different neurodegenerative diseases including Parkinson's disease (PD), Alzheimer's disease (AD), and Huntington's disease (HD). This is remarkable, because the distinct pathological proteins responsible for the different diseases induce the loss of different neural populations. Impaired adult neurogenesis was shown in numerous animal models of neurodegenerative diseases; however, only few postmortem studies have been performed. We will review concepts related to the interplay between cellular plasticity in regions of adult neurogenesis with a specific focus on cell-autonomous and non-cell-autonomous factors. Furthermore, various strategies aimed to stimulate neuronal plasticity will be discussed within the context of a potential translation into therapeutic approaches for neuropsychiatric symptoms associated with PD, HD, and AD.

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Figures

Figure 1.
Figure 1.
Model of effects of human wild-type α-synuclein (WTS) and mouse endogenous α-synuclein in the dentate gyrus (DG). (A) A newly generated neuron integrating into the DG is shown on the left part of all images; the right part depicts a higher magnified insert of a dendrite showing spines and the larger mushroom spines (A–D). (B–D) Models showing the impact of WTS on dendrite and spine development. (B) Platelet-derived growth factor (PDGF) WTS transgenic mice. (C) Retroviral overexpression of WTS using a CAG-WTS-green fluorescent protein (GFP) construct. (D) Retroviral overexpression of WTS on an α/β-synuclein knockout background. Cell-specific overexpression of WTS results in decreased dendrite length and spine density (B,C), whereas nonspecific overexpression (C) leads to a decrease in mushroom spines, as indicated in the purple panels showing an example of magnification of the spines (according to Winner et al. 2012). CAG, Cytomegalovirus (CMV) enhancer fused to the chicken β-actin promoter.
See this image and copyright information in PMC

References

    1. Aarsland D, Marsh L, Schrag A 2009. Neuropsychiatric symptoms in Parkinson's disease. Mov Disord 24: 2175–2186. - PMC - PubMed
    1. Abeliovich A, Schmitz Y, Farinas I, Choi-Lundberg D, Ho WH, Castillo PE, Shinsky N, Verdugo JM, Armanini M, Ryan A, et al. 2000. Mice lacking α-synuclein display functional deficits in the nigrostriatal dopamine system. Neuron 25: 239–252. - PubMed
    1. Altman J 1969. Autoradiographic and histological studies of postnatal neurogenesis: IV. Cell proliferation and migration in the anterior forebrain, with special reference to persisting neurogenesis in the olfactory bulb. J Comp Neurol 137: 433–457. - PubMed
    1. Altman J, Das GD 1965. Autoradiographic and histological evidence of postnatal hippocampal neurogenesis in rats. J Comp Neurol 124: 319–335. - PubMed
    1. Appel-Cresswell S, Vilarino-Guell C, Encarnacion M, Sherman H, Yu I, Shah B, Weir D, Thompson C, Szu-Tu C, Trinh J, et al. 2013. α-Synuclein p.H50Q, a novel pathogenic mutation for Parkinson's disease. Mov Disord 28: 811–813. - PubMed

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